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+ | ==== Ketamine and the Near Death Experience ==== | ||
- | + | (see also http:// | |
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- | ==== Ketamine and the Near Death Experience ==== | + | |
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Endogenous substances have been found in the brain which bind to the PCP receptor, one of which is a peptide called ' | Endogenous substances have been found in the brain which bind to the PCP receptor, one of which is a peptide called ' | ||
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- | + | 1. Depersonalisation | |
- | 1. Depersonalisation | + | |
The depersonalisation theory proposes that the NDE is an adaptive mechanism of the personality which alerts one to the threat of death while potentially overwhelming emotion is held at bay, allowing the reality to be integrated without panic (Greyson, 1983; Noyes and Kletti, 1976a,b). While protecting nerve cells from ischaemic damage is largely irrelevant when one is falling from a cliff, the NDE-producing situation which first resulted in this hypothesis, NMDA receptors would certainly be involved in producing the experience of depersonalisation as they play a central role in cognition and perception. | The depersonalisation theory proposes that the NDE is an adaptive mechanism of the personality which alerts one to the threat of death while potentially overwhelming emotion is held at bay, allowing the reality to be integrated without panic (Greyson, 1983; Noyes and Kletti, 1976a,b). While protecting nerve cells from ischaemic damage is largely irrelevant when one is falling from a cliff, the NDE-producing situation which first resulted in this hypothesis, NMDA receptors would certainly be involved in producing the experience of depersonalisation as they play a central role in cognition and perception. | ||
- | + | 1. Regression in the service of the ego | |
- | 1. Regression in the service of the ego | + | |
This theory maintains that confronting death leads to a cutting off the external world. The result is regression to a pre-verbal level which can be experienced as mystical ineffability (Greyson, 1983). Certainly a loss of contact with the external world is one of the most characteristic effects of ketamine.This is probably the result of blockade of NMDA receptors involved in sensory transmission. NMDA receptors play a key role in the transmission of incoming signals from all sensory modalities (Davies and Watkins, 1983; Greenamyre et al., 1984; Headley et al., | This theory maintains that confronting death leads to a cutting off the external world. The result is regression to a pre-verbal level which can be experienced as mystical ineffability (Greyson, 1983). Certainly a loss of contact with the external world is one of the most characteristic effects of ketamine.This is probably the result of blockade of NMDA receptors involved in sensory transmission. NMDA receptors play a key role in the transmission of incoming signals from all sensory modalities (Davies and Watkins, 1983; Greenamyre et al., 1984; Headley et al., | ||
- | 1. ; Cotman et al., 1987; Cline et al.,1987; Monaghan, Bridges and Cotman, 1988; Kisvardy et al., 1989; Oye et al., | + | 1. ; Cotman et al., 1987; Cline et al.,1987; Monaghan, Bridges and Cotman, 1988; Kisvardy et al., 1989; Oye et al., |
- | 2. ). | + | 2. ). |
- | 1. A state dependent reactivation of birth memories | + | 1. A state dependent reactivation of birth memories |
This theory explains the movement through tunnels towards 'the light' as a memory of being born (Grof and Halifax, | This theory explains the movement through tunnels towards 'the light' as a memory of being born (Grof and Halifax, | ||
- | 1. ). The NDE is thus actually a ' | + | 1. ). The NDE is thus actually a ' |
NMDA receptor blockade could certainly be the underlying mechanism for the release of extremely primitive memories not normally available to consciousness. | NMDA receptor blockade could certainly be the underlying mechanism for the release of extremely primitive memories not normally available to consciousness. | ||
- | + | 1. The NDE as a sensory deprivation phenomenon | |
- | 1. The NDE as a sensory deprivation phenomenon | + | |
This hypothesis maintains that memories may normally be suppressed by a mechanism which acts as a gate, admitting primarily external signals when we are fully conscious and concentrating upon an external task (Siegel, | This hypothesis maintains that memories may normally be suppressed by a mechanism which acts as a gate, admitting primarily external signals when we are fully conscious and concentrating upon an external task (Siegel, | ||
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Ketamine blocks this channel at the molecular level and, at a higher level, closes the ' | Ketamine blocks this channel at the molecular level and, at a higher level, closes the ' | ||
- | 1. ; Cotman, Monaghan and Ganong, 1988). | + | 1. ; Cotman, Monaghan and Ganong, 1988). |
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The hypothesis presented in this paper is that much can be learnt about the mechanisms of the NDE by studying drug-induced hallucinations, | The hypothesis presented in this paper is that much can be learnt about the mechanisms of the NDE by studying drug-induced hallucinations, | ||
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It is also possible that there is no protective mechanism against excitotoxicity. Rather than mimicing a natural protective process, ketamine may have some of its psychological effects by mimicing some of the processes seen in temporal lobe epilepsy. Ketamine does block glutamatergic neuro-transmission and prevents excitotoxic cell death. However, the effect of ketamine upon human electrical brain waves (the electroencephalograph, | It is also possible that there is no protective mechanism against excitotoxicity. Rather than mimicing a natural protective process, ketamine may have some of its psychological effects by mimicing some of the processes seen in temporal lobe epilepsy. Ketamine does block glutamatergic neuro-transmission and prevents excitotoxic cell death. However, the effect of ketamine upon human electrical brain waves (the electroencephalograph, | ||
- | 1. ; Leccese et al., 1986; Mares et al., 1992) and as a pro-convulsant (epilepsy inducing substance) (Bennet et al., 1973; Gourie et al., 1983; Myslobodsky, | + | 1. ; Leccese et al., 1986; Mares et al., 1992) and as a pro-convulsant (epilepsy inducing substance) (Bennet et al., 1973; Gourie et al., 1983; Myslobodsky, |
The hippocampus is one of the core structures in the limbic system. Thus the production of NDE's by ketamine is not inconsistent with the hypothesis that NDE's may result from abnormal electrical activity in the brain. Reich and Silvay (1989) concluded: " it is hard to draw objective conclusions regarding the anti-convulsant properties of ketamine...animal data are particularly difficult to interpret because of interspecies variations" | The hippocampus is one of the core structures in the limbic system. Thus the production of NDE's by ketamine is not inconsistent with the hypothesis that NDE's may result from abnormal electrical activity in the brain. Reich and Silvay (1989) concluded: " it is hard to draw objective conclusions regarding the anti-convulsant properties of ketamine...animal data are particularly difficult to interpret because of interspecies variations" | ||
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(+)ketamine is about four times more potent as a hypnotic (sleep-inducing agent) and analgesic, and has different effects upon the EEG from (-)ketamine (White et al., 1985). This may explain some of the confusion concerning whether ketamine is an anticonvulsant or a proconvulsant (Myslobodsky et al.,1981), and suggests that future NDE research might be better done with (-)ketamine rather than the mixture currently supplied to anaesthetists. | (+)ketamine is about four times more potent as a hypnotic (sleep-inducing agent) and analgesic, and has different effects upon the EEG from (-)ketamine (White et al., 1985). This may explain some of the confusion concerning whether ketamine is an anticonvulsant or a proconvulsant (Myslobodsky et al.,1981), and suggests that future NDE research might be better done with (-)ketamine rather than the mixture currently supplied to anaesthetists. | ||
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- | 1. Hypoxia (low oxygen): | + | 1. Hypoxia (low oxygen): |
The proposal that lack of oxygen might precipitate NDE's (Blacher, 1980) has been criticized (e.g. Sabom, 1982) because experiments in which the inspired oxygen was made to fall slowly resulted in mental clouding rather than states of consciousness resembling the NDE (Henderson et al., 1927). However, these experiments are clearly not a satifactory reproduction of events in, for example, cardiac arrest, a drug overdose or other types of medical emergency associated with NDE's. Hypoxia has been clearly shown to cause an excessive release of glutamate with resulting excitotoxicity and cell death, which can be prevented by ketamine (see previous references). | The proposal that lack of oxygen might precipitate NDE's (Blacher, 1980) has been criticized (e.g. Sabom, 1982) because experiments in which the inspired oxygen was made to fall slowly resulted in mental clouding rather than states of consciousness resembling the NDE (Henderson et al., 1927). However, these experiments are clearly not a satifactory reproduction of events in, for example, cardiac arrest, a drug overdose or other types of medical emergency associated with NDE's. Hypoxia has been clearly shown to cause an excessive release of glutamate with resulting excitotoxicity and cell death, which can be prevented by ketamine (see previous references). | ||
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- | 1. Hypercarbia (excessive CO2): | + | 1. Hypercarbia (excessive CO2): |
In experimental paradigms, CO2-enriched breathing mixtures can result in NDE phenomena such as bodily detachment, being drawn towards a bright light etc. As with NDE's, diverse personality types report similar experiences, | In experimental paradigms, CO2-enriched breathing mixtures can result in NDE phenomena such as bodily detachment, being drawn towards a bright light etc. As with NDE's, diverse personality types report similar experiences, |